STEPTRACKERCARDIOVASCULAR | PATHOLOGY | HIGH-YIELD REVIEW

Ischemic Heart Disease

Oxygen supply can't meet demand — stable plaque, ruptured plaque, spasm or sudden arrhythmia.

FOCUS ON
Sort by mechanism and ECG. Stable angina: fixed plaque, pain on exertion. Unstable angina / NSTEMI: partial thrombus, ST depression; troponin separates them. STEMI: complete occlusion, ST elevation. Prinzmetal: spasm with transient ST elevation. Match ECG leads to coronary arteries.
SYNDROME
MECHANISM
FEATURES
ECG · LABS · TREATMENT
Stable angina
Fixed stenosis > 70% → demand ischemia of subendocardium.
Exertional or emotional chest pressure < 20 min, relieved by rest or nitroglycerin
ST depression during pain; troponin normal · nitrates, β-blockers, aspirin, statin
Unstable angina
Plaque rupture with a non-occlusive thrombus.
Pain at rest, new, or crescendo pattern
ST depression/T inversion; troponin normal; high MI risk
NSTEMI
Partial occlusion → subendocardial infarct.
Rest pain, often longer
ST depression; troponin ↑
STEMI
Complete occlusion → transmural infarct.
Severe pain, diaphoresis, nausea, dyspnea; may be silent in diabetics and elderly
ST elevation or new LBBB; troponin ↑ · PCI within 90 min or fibrinolysis within 12 h
Prinzmetal (vasospastic) angina
Coronary spasm, often without fixed disease.
Rest pain at night/early morning; young smokers; cocaine, triptans, ergots
Transient ST elevation · CCBs, nitrates; avoid non-selective β-blockers
Sudden cardiac death
Death within 1 hour of symptoms, usually ventricular fibrillation.
Adults: acute ischemia from CAD · young: HCM, long QT, Brugada, myocarditis
Athlete collapsing on the field → think HCM
Chronic ischemic heart disease
Repeated ischemia and post-MI remodeling.
Progressive heart failure
Ischemic cardiomyopathy
Coronary steal
Vasodilators (adenosine, dipyridamole) dilate healthy vessels and divert flow from stenotic beds.
Provoked ischemia
Basis of pharmacologic stress testing

Mechanism — supply vs demand

Demand ↑Exercise, tachycardia, HTN
→
Supply ↓Plaque, thrombus, spasm
→
Subendocardium firstFarthest from epicardial vessels
→
ST depressionPartial-thickness
→
Total occlusionTransmural → ST elevation

The LAD is the most commonly occluded artery, followed by the RCA and then the left circumflex.

Coronary territories

ARTERY
WALL
ECG LEADS
LAD
Anterior wall, anterior septum, apex
V1–V4
Left circumflex
Lateral wall
I, aVL, V5–V6
RCA
Inferior wall; SA and AV nodes (most people); posteromedial papillary muscle
II, III, aVF
Posterior (PDA)
Posterior wall
ST depression V1–V3 (reciprocal)
Left main
Large anterolateral territory
Widespread changes; aVR elevation

How it's tested

COMMON CONFUSIONUnstable angina and NSTEMI can share the same ECG. Only troponin separates them.
THE TRAPChest pain in a cocaine user is vasospasm plus a sympathetic surge. Benzodiazepines, nitrates and CCBs come first; avoid a non-selective β-blocker, which leaves α-vasoconstriction unopposed.
YOUR APPROACHPain pattern (exertional vs rest) → ECG (depression vs elevation) → troponin → territory from the leads.

If you see… think…

Exertional chest pressure relieved by rest → stable angina
New rest pain, ST depression, normal troponin → unstable angina
ST depression + rising troponin → NSTEMI
ST elevation in II, III, aVF + bradycardia → inferior MI (RCA)
ST elevation V1–V4 → LAD occlusion
Young smoker, early-morning pain, transient ST elevation, clean coronaries → Prinzmetal angina
Chest pain after cocaine → vasospasm — avoid non-selective β-blockers
Young athlete collapses and dies → hypertrophic cardiomyopathy
Ischemia provoked by dipyridamole → coronary steal